Diarrhea is the frequent evacuation of watery stools. Vomiting is the forceful expulsion of stomach contents through the mouth. 

What to Do

1. Remove all food and water. 
2. Check for signs of dehydration. 
3. If diarrhea and/or vomiting continues or the pet acts ill, seek veterinary attention. 
4. If no vomiting occurs for 6 to 8 hours, begin to frequently give small amounts of clear liquids (water, Gatorade, Pedialyte, or other electrolyte solution).
   • A rule of thumb is to give 1 teaspoon per pound of body weight every 2 or 3 hours throughout the day and night. 
   • If your pet does not vomit the fluid, the following day offer small frequent meals of boiled hamburger and rice or boiled chicken and rice.
5. If your pet does not want to eat, starts to vomit, or continues to have diarrhea, see a veterinarian right away.
6. Isolate the sick pet from other pets.

Diarrhea and vomiting can quickly lead to serious fluid loss and electrolyte imbalance, especially in very young or old animals, and those with certain health issues.  Severely dehydrated animals may need to be hospitalized and receive IV fluids to recover.

What NOT to Do

• Do not administer any over-the-counter or prescription medications to your pet without talking to a veterinarian first.  
• Do not allow the pet to eat or drink anything until there has been no vomiting for 6 to 8 hours.

Most infections that cause diarrhea and vomiting are contagious, so it is wise to assume that other pets might be vulnerable if they are exposed. 

If your pet is not feeling well and has vomiting and/or diarrhea, see a veterinarian.

Skin Glands: Dogs do not produce sweat to cool off. However, dogs do have sweat glands, called apocrine glands, associated with each group of hairs. Apocrine glands likely produce pheromones, or chemical signals, for communication with other dogs.

Dogs also have another type of sweat glands, called eccrine glands, on the pads of their paws and on their noses, which help keep these areas moist and functioning properly. On the paw pads, natural micro-organisms live in the surface layers and contribute to the paw’s typical odor – like cheese puff snacks or Fritos! This odor is much more noticeable on dogs with moist paw pads than on those with dry pads.

Dogs also have numerous glands, called ceruminous glands and sebaceous glands, in their external ear canals. Together these two sets of glands produce natural ear wax, or cerumen. Micro-organisms live naturally in this material and give the ears a slightly yeasty odor even when ears may be healthy.

Dogs, like all carnivores, have two scent glands called anal sacs that communicate with the surface of the skin by ducts that open on either side of the anus. They produce a natural secretion that varies from thin and yellowish to pasty and grayish. Anal gland secretions may have a very strong musty odor. A small amount of this material is normally deposited when dogs defecate and a large amount may be extruded when a dog is frightened. This secretion is thought to leave a signal to other dogs telling them who left fecal deposit. This odor is also the signal being sampled when strange dogs investigate one another by sniffing out the anal area.

Another source of odor that can be considered natural results from a common dog behavior. Dogs like to roll in and mark themselves with animal products in their environment, including fecal deposits of natural prey animals. One of their favorites is rabbit droppings. This might be a method of communicating with pack members about the other animals that are active in the pack home territory, a behavior left over from ancestor wolves.

Un-natural Sources of Odor on Pet Dogs

Poor grooming: Some dogs, especially those with long, thick or corded hair, need regular grooming. A coat that is not kept clean and groomed can trap dirt and other substances with unpleasant odors. If a dog’s haircoat is chronically wet, it can harbor lots of bacteria and yeast. 

Skin diseases: Dogs with allergies (allergic dermatitis, atopic dermatitis) may have a musty odor. This is because allergies can cause increased sweating (hyperhidrosis), bacterial skin infections (bacterial dermatitis or pyoderma) and yeast skin infections (Malassezia dermatitis). Dogs with seborrhea, a type of keratinization defect, and dogs with deep skin folds are also prone to bacterial and yeast skin infections.

Ear diseases: Ear infections, or otitis are a common source of odor in dogs.  The smell can be yeasty or actually smell like sewage.

Anal sac diseases: Excessive anal gland secretion can result in a musty, pungent odor. Anal sacs can also become abscessed or infected, with bacteria or yeast organisms then producing an odor.

Dental disease: Various dental diseases can cause bad breath, or halitosis. Dental calculus harbors numerous bacteria that produce odor. Dental disease can also lead to excessive drooling, causing the skin around the mouth to become infected and odiferous.

Medications: Some medications, especially antibiotics or medicated shampoos, have odors that owners may find unpleasant. Chlorhexidine is a common disinfectant incorporated in skin medications that some people find has an unpleasant smell.

Diet: Some dog foods based on fish meal or with added fish oil can make for fishy-smelling dogs.

Flatulence: The overproduction of intestinal gas can be a problem for some dogs.  This may be diet-related or a sign of gastrointestinal disease. 

Skunks: Dogs and skunks don’t mix well and a dog may be sprayed in the encounter. This results in an over-powering musky acrid odor that remains apparent in the ‘skunked’ dog’s coat for many days or even weeks until steps are taken to neutralize the odor.

In some cases, the tendency to develop demodectic mange runs in families.

Signs of demodicosis can include hair loss, reddened skin, scabbing, crusting and sometimes itching.

Localized demodicosis involves only small areas of skin on a dog. Generalized demodicosis involves most of a dog’s body or paws. Skin infections from mite damage are common. Sometimes, these skin infections become life-threatening, and cause swelling and fever.

Any skin infection needs to be treated with a topical medication or antibiotic. For localized demodicosis, most dogs resolve on their own and don’t need to be treated with an anti-mite medication. Instead, dogs with localized demodicosis are observed for spreading or worsening of mites. For dogs with generalized demodicosis, treatment requires an anti-mite medication such as one of the following below. Continue any anti-mite treatment until no mites are found on two consecutive skin scrapings.

Dips are usually applied either weekly or every two weeks according to the veterinarian’s prescription. Dips are usually applied by grooming technicians in the veterinarian’s hospital.

Occasionally, another form of amitraz (Taktic®) is chosen. Different dilution instructions are required for Taktic®.

Ivermectin

Ivermectin is available as a liquid deworming agent (Ivomec® and generics) and as a monthly heartworm preventative pill. For canine demodicosis, the liquid form is given by mouth once a day. Side effects can include the following: lethargy, vomiting, diarrhea, and neurologic signs. Many veterinarians will gradually increase the dose of ivermectin to monitor for side effects. Side effects are more common in herding breed dogs (e.g. Collies, Border collies, and Old English sheepdogs). A genetic test is also available to determine if a dog may be sensitive to ivermectin.

Milbemycin oxime

Milbemycin is available as a monthly heartworm preventive pill (Interceptor®) for dogs. For canine demodicosis, the pill is given by mouth once a day.  Side effects can include the following: lethargy, vomiting, diarrhea, and neurologic signs.

Moxidectin

Moxidectin is available as a liquid deworming agent and as a monthly topical heartworm preventative (Advantage Multi®). For canine demodicosis, usually the topical form is applied to the skin once a week.  Side effects can include the following: lethargy, vomiting, diarrhea, and neurologic signs.

The Isoxazoline Flea/Tick Products (Bravecto®, Nexgard®, and Simparica®)
These medications are available as oral flea and tick control pills for dogs. For canine demodicosis, the dose varies based on the specific product.

Many veterinarians will neuter dogs with generalized demodicosis as soon as the disease is under control. This is in the best interest of the dog since breeding and heat cycles can cause disease recurrence. Additionally, veterinarians recommend neutering dogs with juvenile-onset, generalized demodicosis because this disease likely has a genetic basis.  

Animals with localized demodicosis have a good prognosis with proper care. As the severity of the disease increases, the prognosis worsens. Some dogs with generalized demodicosis must have regular treatment for the rest of their lives while others may be cured after a variable number of months of treatment. In all cases it is important to keep your pet as healthy and stress free as possible, including a good nutritional diet, regular checkups, routine deworming and heartworm prevention.

The Culprit – Demodex Canis

Most dogs live in harmony with their mites, never suffering any consequences from being parasitized. If, however, conditions change to upset the natural equilibrium (such as some kind of suppression of the dog’s immune system), the Demodex mites may gain the upper hand. The mites proliferate and can cause serious skin diseases.

Is Demodicosis Contagious?

Unlike sarcoptic mange, demodectic mange is not considered a contagious disease, and isolation of affected dogs is generally not considered necessary. That said, there are some circumstances under which the mites could spread from one dog to another. Classically Demodex mites have been felt to only be transferable from mother to newborn pup. After the pup is a week or so old, it has developed enough immunity so that infection is no longer possible. In other words, after age one week or so, a dog will no longer accept new mites on its body. Recently this idea has been challenged as occasionally multiple unrelated dogs break with demodicosis in the same household. It is not clear if some species of Demodex are more contagious than others or if some contagion is possible under certain circumstances. Current thinking is that mites actually can be transferred from one dog to another but as long as the dog is healthy, the mites simply add into the dog’s natural mite population, and no skin disease results. In rare circumstances, the spread of disease is possible if severe infection is involved. While there are still assorted theories about dog-to-dog transmission of Demodex mites, there is no question that mites cannot be transmitted to humans or to cats.

• Mites live inside hair follicles — a difficult place for miticides (chemicals that kill mites) to reach.
• Mites are normal residents of dog skin; it is only in some individual dogs that mites cause problems.

Demodicosis Has Three Forms

Form #1: Localized

Localized demodicosis occurs as isolated, scaly bald patches, usually on the dog’s face, creating a polka-dot appearance. Localized demodicosis is considered a common puppyhood ailment, and approximately 90% of cases resolve with no treatment of any kind. This is quite a contrast to generalized demodicosis, as described below, so it is important to be able to distinguish localized from generalized disease. It seems like this would be a simple task since localized demodicosis classically involves several round facial bald spots, and generalized demodicosis involves a bald scaly entire dog; still, reality does not always fit into neat categories in this way. Some guidelines used to distinguish localized demodicosis include:

• Localized disease does not involve more than two body regions. (One spot or two on the face and one spot or two on a leg would still qualify as localized even though the spots are not close together.)
• Localized disease involves no more than four spots total on the dog.

Not all flea products will kill Demodex; one needs a product of the isoxazoline class, and the puppy must be old enough for such a product. 

If there is a reason why the puppy cannot take an isoxazoline flea product, there are alternatives. Goodwinol ointment, an insecticide ointment, may be used daily to control localized demodicosis. Antibacterial gels are also used against localized demodicosis and associated skin infections. It is important to note that rubbing a creme or ointment on a demodicosis lesion can cause reddening of the lesion, making it appear to get worse. It is also possible for rubbing the medication on the area to break off the weaker hairs at the margin of the lesion, causing the lesion to appear to get bigger. Neither of these situations truly represents an exacerbation of the disease.

Without treatment, the resolution of a localized demodicosis lesion should be at least partially apparent after one month though total resolution can take up to three months.

Approximately 10% of localized demodicosis cases will progress to generalized demodicosis. Enlarged lymph nodes are a bad sign — often foretelling generalized mange.

Can the Pup be Bred Later?

Sometimes the puppy with localized demodicosis was obtained for breeding purposes. The current recommendation is not to treat these puppies so that we can determine if the condition will stay localized and resolve or if it will generalize. If it stays localized and eventually resolves without treatment, the animal is still a candidate for breeding. If the condition generalizes to cover the entire body, the animal should be sterilized. If the condition receives treatment and resolves, we will never know how the disease would have gone in its natural state and will not know whether the pup is carrying the genetic predisposition for generalized demodectic mange. In this case, it is best to be conservative and not take the chance of passing on genetic predisposition for this disease.

Localized demodicosis is almost exclusively a puppyhood disease. When a puppy develops localized demodicosis the chance of the condition resolving is 90% unless there is a family history of demodicosis in related dogs. In this case, the chance of spontaneous resolution drops to 50%.

Occasionally an adult dog develops localized demodicosis. We currently do not have a good understanding of the prognosis or significance of this condition in an adult dog.

It is important that dogs with a history of generalized demodectic mange not be bred, as there is a hereditary component to the disease.

Form #2: Generalized

The secondary bacterial infections make this a very itchy and often smelly skin disease. These infections may require antibiotics but it is important to realize that infection will probably not resolve fully until the mites are gone.

The goal of treatment is the total eradication of the mite population on the dog’s body.

Juvenile Onset (The Most Common Form)

Young dogs that develop demodicosis are believed to have a genetic immunological defect that allows the mite to gain the upper hand. As the puppy grows up and his or her immune system matures, the immune system tends to naturally regain control of their mite infestation; in fact, 30-50% of dogs under age 1 year recover spontaneously from generalized demodicosis without any form of treatment. Usually, treatment is recommended, though, to facilitate recovery.

Adult Onset

Most demodicosis occurs in young dogs under age one and a half. An older dog should not get demodicosis unless there is an underlying problem with the immune system. In such cases, demodicosis is considered an indication to seek a more serious hidden condition such as cancer, liver or kidney disease, or an immune-suppressive hormone imbalance. A more extensive medical work-up will be required. In the case of shelter dogs, sometimes the stress of abandonment, street living, starvation or other poor husbandry can compound into the immune suppression needed to generate a case of adult-onset demodectic mange.

Years ago, generalized demodicosis was nearly untreatable, and many dogs were euthanized for uncontrollable disease. Today, treatment for most dogs is surprisingly simple.

Treatment

The biggest change in treating this condition came, as mentioned, with the release of the isoxazoline flea products (sarolaner/Simparica®, fluralaner/Bravecto®, afoxalaner/Nexgard®, lotilaner/Credelio®). The isoxazoline products are oral medications labeled to kill fleas and ticks in dogs. It turns out they have substantial activity against Demodex mites and are successful enough that they have become the treatment of choice. These products are typically given orally every two to four weeks, depending on the protocol. Most dogs are simply cured by this protocol.

Occasionally, a dog fails this treatment and is relegated to the more traditional methods such as high-dose oral ivermectin, a protocol that is not safe for many herding breeds; topical moxidectin (Advantage multi®); daily oral milbemycin (Interceptor®); or even labor-intensive dipping with amitraz (Mitaban®).

The common anti-itch medication oclacitinib (Apoquel®) is an immunosuppressant and thus decreases the body’s ability to fight the Demodex infection. Understand before you use it to treat the itch of the Demodex infection that it can make the mites worse. Other forms of itch relief should be sought if necessary. Oclatacinib use can actually lead to a recurrence of demodicosis years after recovery, so it should not be used in any dog that has ever suffered from demodicosis previously.

Prognosis

The younger the dog, the better the chance of cure. Most dogs under one-and-a-half years of age recover completely from generalized demodicosis. In many cases of adult-onset demodicosis, the disease is controlled with treatment, but a cure is not always possible. Some cases can never be controlled.

No matter which option you choose, treatment should be accompanied by skin scrapes every two to four weeks. In this way, the effectiveness of treatment is assessed, and dosing can be changed. There are several protocols describing how to determine if treatment can be stopped. The idea is to eradicate every single mite from the dog’s body so that the condition cannot recur. This typically entails either continuing treatment for a significant time after the patient appears recovered and/or rechecking skin scrapes a significant time after treatment is finished.

Relapse?

When relapse occurs, it is often because the dog appeared to be normal, and treatment was discontinued before all Demodex mites were killed off. Relapse is always a possibility with generalized demodicosis as there is no easy way to confirm that every mite has been killed, but most dogs that relapse do so within a six to 12-month period from the time they appear to have been cured.

Sarcoptic mange is a completely different disease.

We Wish it Weren’t Necessary to Add This

Decades ago, dipping dogs with demodectic mange in motor oil was a popular home remedy. However, skin exposure to motor oil can cause rashes and skin destruction in severe cases. The hydrocarbons can be absorbed through the skin and cause a dangerous drop in blood pressure. If motor oil is licked off the coat, resultant vomiting can lead to aspiration of motor oil into the lungs and pneumonia. Kidney and liver damage can result from motor oil dipping.

Form #3: Demodectic Pododermatitis

It is one of the most resistant forms of demodicosis, and deep infections and proliferative tissue that result can take months and great expense to resolve.

In the past, special organophosphate foot soaks, along with daily medications, were needed to resolve this condition, and months of treatment were common. As with the other forms of demodicosis, the isoxazoline flea products (sarolaner/Simparica®, fluralaner/Bravecto®, afoxalaner/Nexgard®, lotilaner/Credelio®) have changed everything. In most cases, the mites can be quickly killed, and the deep secondary infections can be resolved in a matter of weeks (instead of months) once the mites are gone. 

Examination is the key to diagnosis and helps determine the type of treatment needed. The veterinarian needs to know what to look for. A pet owner can help by examining their pet’s teeth and mouth at least monthly.First, smell your pet’s breath. If you sense a disagreeable odor, your pet may have gum disease. Periodontal disease is the most common ailment of small animals and is treatable.  Gum problems begin when bacteria accumulate at the gumline around the tooth. Unless brushed away daily, these bacteria can destroy tooth-supporting bone, and cause bleeding, and tooth loss. Usually, the first sign is bad breath.

When examining your pet’s mouth, look for tooth chips or fractures on the tooth’s surface. Contrary to their popularity, chewing on cow hooves, antlers, rocks, bones, or other hard materials may break teeth. If the fracture is deep you may notice a red, brown, or black spot in the middle of the tooth’s surface. The spot is the tooth’s nerve and inside vessels, which when exposed to the oral cavity may eventually lead to a tooth painful abscess.

When your home exam reveals dental problems or if you are still uncertain, a trip to the veterinarian is in order. The veterinary oral examination will begin with a complete visual examination of the face, mouth, and each tooth. Frequently pets’ mouths have several different problems that need care. The veterinarian will usually use a record chart similar to the one used by human dentists to identify and document such dental problems.

A more detailed exam then follows. Unfortunately, cats and dogs cannot point to dental abnormalities with their paws, and to determine the proper treatment plan, other tests are usually necessary. General anesthesia is essential for a proper tooth-by-tooth evaluation. There is a wide array of safe and effective anesthetics and monitoring equipment that make anesthesia as safe as possible.

Expect your veterinarian or dental assistant to use a periodontal probe to measure gum pocket depths around each tooth. One or two millimeters of probe depth normally exists around each tooth. When dogs or cats are affected by periodontal disease, the gums bleed and probing depths may increase, which requires additional care to save the teeth. Unfortunately by the time some pets come in for dental care, it is too late to save all of the teeth. Your veterinarian may also take x-rays of the entire mouth. X-rays show the inside of the tooth and the root that lies below the gum line. Many decisions are based on x-ray findings. Usually, the veterinarian will visually examine the mouth, note any problems, take X-rays under anesthesia, and then tell you what needs to happen to treat the problems found if any.

Plaque removal and preventative care with periodic checkups should help hinder the loss of additional teeth. Plaque and tartar preventative products can be found at the Veterinary Oral Health Council. 

If your dog or cat needs advanced dental care, where can you go?

Many veterinarians have taken post-graduate dental training in order to better serve their patients. Some veterinarians have passed advanced written and practical examinations given by the American Veterinary Medical Association, which certifies them as dental specialists. If you need one, your veterinarian can refer you.

Dogs and cats do not have to suffer the pain and discomfort of untreated broken or loose teeth or infected gums. With the help of thorough examinations, x-rays, dental care, and daily plaque prevention, your pet can keep his teeth in his mouth where they should be.

When the myocardium cannot pump blood out of the left heart effectively, the kidneys retain sodium and water to increase the amount of blood returning to the heart. This leads to an enlargement of the ventricles in order to compensate for the ineffective pumping. This is helpful for years, but ultimately becomes detrimental when it causes the blood pressure in the heart to back up into the lungs, thereby causing fluid accumulation within the lungs (pulmonary edema). This is called heart failure or congestive heart failure (CHF).

Although less common, DCM affecting the right ventricle can also occur. Blood backs up on the right side, which receives blood from the body and pumps it to the lungs, resulting in right-sided CHF, where fluid accumulates in the abdomen (ascites) and chest (pleural effusion). DCM affecting the right ventricle is almost always accompanied by DCM of the left ventricle.

What Breeds get DCM?

There are several breeds that are predisposed to DCM. These include Doberman Pinschers, Great Danes, Irish Wolfhounds, Boxers, Newfoundlands, Portuguese Water Dogs, Dalmatians and Cocker Spaniels.  DCM is not just limited to specific breeds. Large and giant breeds are most commonly affected, but it also occurs in smaller breed dogs and cats as well.

The causes of DCM in these breeds vary, as explained below.

What Causes DCM?

Because of the strong breed association, DCM almost certainly is inherited in many breeds. Genetic mutations that are associated with DCM have been identified in Doberman Pinschers, Boxers and Standard Schnauzers. Genetic testing for these mutations can be done for each.

Boxers get a specific type of cardiomyopathy called arrhythmogenic right ventricular cardiomyopathy (ARVC). Approximately 90% of these dogs in the USA have a ventricular arrhythmia and an otherwise normally functioning heart. They are prone to fainting and sudden death. The fainting most commonly happens when they develop a very fast heart rate (greater than 400 beats/min). Sudden death usually occurs when this fast rate degenerates into ventricular fibrillation (cardiac arrest). Approximately 10 percent also get DCM as a part of their disease. The disease is associated with a genetic mutation in a gene called striatin.

In some dogs, DCM is due to a nutritional deficiency. Taurine is an amino acid required for the development and function of the myocardium. Consequently, pets may develop DCM on taurine-deficient diets, such as vegetarian diets, and may benefit from appropriate supplementation. Some breeds, such as American Cocker Spaniels and Golden Retrievers, may have a predisposition to taurine-deficiency, possibly through defects in metabolizing taurine. Many, but not all, cases that are supplemented with taurine will improve. Some also need carnitine supplementation. If your pet is diagnosed with DCM, testing for a taurine deficiency may be warranted. Breeds such as Doberman Pinschers and Great Danes do not have taurine-deficient cardiomyopathy. Some cats may develop taurine-deficient DCM, although this has become rare as taurine is now added to virtually all quality cat foods (see Feline Cardiomyopathy).

L-carnitine is another amino acid that has rarely been implicated in the development of DCM in people. L-carnitine is required for the myocardial cells to produce energy and thus contract. There is some evidence that a deficiency in this molecule will contribute to myocardial dysfunction in Boxers (one small study only). Some American cocker spaniels need to be supplemented with it, along with taurine, to produce a beneficial response. However, the role of carnitine in most DCM cases is very limited.

In 2018, grain free diets were implicated in causing DCM in dogs, especially in breeds that do not typically get DCM.  Read more details about this potential cause.

Occasionally, toxins can cause DCM. The most common toxin is doxorubicin (Adriamycin), an anti-cancer drug used to treat various cancers in dogs. In some cases, dogs receiving doxorubicin  will develop DCM.

Infectious causes of DCM are rare. Puppies infected with parvovirus at two to four weeks of age can develop DCM. These days, vaccinating the mother protects the puppies against parvovirus during this susceptible period, so this cause of DCM is rarely seen. Chagas disease (Trypanosomiasis) can cause DCM in geographic areas where it is found (Texas, Mexico).

What are the Signs of DCM?

Signs of DCM vary depending on the breed of dog and stage of the disease. Loss of appetite, pale gums, increased heart rate, coughing, difficulty breathing, periods of weakness, and fainting are signs commonly seen. Since blood is backed up into the lungs, respiratory signs (CHF) due to pulmonary edema are most common. Blood returning to the right side of the heart from the body may also back up leading to fluid accumulation in the abdomen (ascites) or in the chest cavity (pleural effusion). Weakness or collapse may be caused by abnormal heart rhythms (arrhythmias) and occasionally, decreased blood flow to the body (depressed cardiac output).

In some breeds, sudden death or fainting can occur well before any signs of CHF.

How is DCM Diagnosed?

There are two different methods used to diagnose pets: (A) during a screening exam of an apparently normal dog (e.g. as part of a breeding program), and (B) during examination of a dog with clinical signs of heart disease.

Screening Exams for DCM

Many conscientious breeders and owners of dogs that are predisposed to DCM screen their pets for heart disease to try to minimize the risk of transmitting the disease to offspring. Screening for DCM in dogs can be expensive and complex. The screening test of choice depends on the breed of the dog and the stage of the disease.

The first step is a good physical examination. In most cases, the physical examination is completely normal. Occasionally, the veterinarian may detect an arrhythmia (abnormal heart rhythm). In Doberman Pinschers and Boxers, a 24-hour ECG recording using a 24-hour ambulatory ECG monitor (Holter monitor) is often the best way to screen dogs for early signs of DCM since an abnormal rhythm often occurs before any detectable changes in myocardial contractility. An echocardiogram (an ultrasound scan of the heart) is also used to identify dogs with DCM before they develop clinical signs, but many dogs with mild disease have equivocal findings. This examination is best performed by a board certified veterinary cardiologist.

Genetic testing should be done by breeders of the specific breeds where a mutation or mutations have been identified.

Diagnosis in Dogs with Clinical Signs

A thorough physical examination by your veterinarian, coupled with your pet’s clinical signs and specific breed, may help make the presumptive diagnosis of DCM. Tests that help support the diagnosis are an ECG (electrocardiogram) and x-rays (radiographs) of the chest. The ECG may show an arrhythmia and/or an elevated heart rate. The chest radiographs may show an enlarged heart and/or fluid in the lung tissue or chest cavity. Some dogs may have normal chest radiographs, but have arrhythmias on their ECG. These pets may be in the early stages of DCM (see above).

In dogs with clinical signs of heart failure, an echocardiogram is necessary to confirm the diagnosis of DCM. With an echocardiogram, a cardiologist can visualize the heart and assess its function. A decrease in heart pumping function (contraction) means that the patient has DCM. Your veterinarian may also perform blood tests to look for any underlying nutritional or infectious conditions if the specific case warrants such investigation.

How is DCM Treated?

Treatment of heart failure is based each individual patient. Drugs commonly used are diuretics (most commonly furosemide), ACE inhibitors, and pimobendan. The diuretic forces the kidneys to excrete more sodium and water. It is used to eliminate pulmonary edema (fluid in the lungs) and so improve breathing and/or effusion (fluid accumulation in the chest or abdominal cavities). Pimobendan increases the force of contraction of the ventricles and dilates blood vessels. Both furosemide and pimobendan are effective treatments that prolong survival and improve quality of life.

Pimobendan might increase the time until onset of heart failure in Doberman Pinschers with DCM when given prior to the onset of heart failure.

Management of arrhythmias is often an important part of managing DCM. Dogs with atrial fibrillation are most commonly treated with a combination of digoxin and diltiazem in order to reduce the heart rate. Sotalol alone or in combination with other antiarrhythmic drugs is used in Boxers and in some Doberman Pinschers to suppress ventricular premature complexes and tachycardia in order to stop the dog from fainting and from dying suddenly. Mexiletine is also commonly used in Doberman Pinschers.

In nutritional DCM, specific supplements will be prescribed. Patients with right-sided heart failure will also have fluid physically removed from the abdomen and/or chest cavity by the veterinarian to make the patient more comfortable.

In humans, DCM patients usually get heart transplants. However, this option does not exist for veterinary patients. Other surgical procedures have been evaluated, but currently none are being offered for patient care.

What is the Prognosis of a Pet Diagnosed with DCM?

Unfortunately, in most cases DCM is a progressive, irreversible, and ultimately fatal disease. Survival depends on the stage of disease, the breed of the patient, the specific type of DCM that patient has, and patient/owner treatment compliance. In taurine-deficient DCM, correcting the deficiency in cats results in complete cure. In dogs, correcting the deficiency may result in at least partial reversal of the disease and prolonged survival; however, some cases relapse after several years.

DCM is a slowly progressive disease. If it is diagnosed in the early stages, the patient may live several years before developing clinical signs. In some breeds, such as Doberman Pinschers, sudden death accounts for 30 percent of the deaths from DCM, well before these dogs ever develop CHF.

In other breeds with DCM, such as Doberman Pinschers and Great Danes, in dogs showing clinical signs of CHF medical therapy can help prolong survival. Historical average survival for Doberman Pinschers with clinical DCM was two to three months. However, with pimobendan, recent studies have seen extended survival for this breed to one year. Less is known about outcomes of other breeds with DCM. Once the diagnosis of DCM is made, ask your veterinarian to discuss your pet’s prognosis on an individual basis.

Can I do Anything to Prevent DCM or Slow its Progression?

Currently, the primary intervention that has been shown to alter the course of DCM is nutritional supplementation in dogs with a nutritional deficiency (i.e., taurine deficiency). Since the majority of cases are thought to be genetic, breeding from lines unaffected by the disease helps reduce the chance of inheriting DCM. Genetic tests, when they are available, are of value in determining breeding strategies. In Doberman Pinschers, pimobendan has been reported to prolong a composite survival endpoint although it did not prolong the time until the onset of heart failure and did not prolong the time until sudden death.

What about Other Supplements?

Multivitamin supplements, nutritional supplements, Co-enzyme Q10, and non-Western herbal supplements have all been used for DCM, but none have been examined critically to determine if they hurt or help patients. Use of these supplements is best discussed with your veterinarian.

Setting the Scene for DIC

The patient must already have a serious problem before DIC sets in. Typical conditions that are associated with DIC include those involving dying internal tissue, widespread inflammation, red blood cell destruction, poor circulation, particulate matter in the bloodstream, or loss of blood vessel integrity.

The following conditions are associated with disseminated intravascular coagulation:

• Pancreatitis
• Rattlesnake bite
• Immune mediated hemolytic anemia
• Immune mediated platelet destruction (thrombocytopenia)
• Hemangiosarcoma
• Blood transfusion reaction
• Severe liver failure
• Overwhelming infection (sepsis)
• Crushing injury
• Heatstroke
• Protein-losing enteropathy
• Glomerular disease
• Heartworm disease
• Cushing’s disease

DIC is primarily a canine problem but can occur in cats. The usual underlying causes in feline patients are lymphoma, hepatic lipidosis, and feline infectious peritonitis.

In the normal body, there are small bleeds occurring regularly as we bump into things or cut ourselves. Blood clots patch these small blood vessel tears up and as healing takes place other blood mechanisms dissolve the old clots leaving scar tissue.

In DIC, the normal clotting mechanism is exaggerated. In the normal body, a substance called antithrombin (formerly called antithrombin III) is involved in dissolving old blood clots but in the event of exaggerated clotting, antithrombin becomes prematurely depleted. There are other anti-clotting proteins that are also depleted by the exaggerated clotting state. The result of this depletion is an excess of fibrin, the material of which blood clots are made.

Active proteins involved in the manufacture of fibrin stimulate the blood vessel cells to release inflammatory biochemicals (note: the patient likely started with a disease involving widespread inflammation). Ultimately, there is both inappropriate clotting and bleeding at the same time.

Recognizing DIC

The sooner DIC is recognized, the more likely the chance of a positive outcome. At first, there are no signs at all, just subtle blood test changes. It is important for the medical staff to watch for these lab changes in patients known to have diseases associated with DIC.

There are several factors that go into the diagnosis of DIC and a patient need not have them all:

Low platelet count

Platelets are the white blood cell fragments that are involved in normal blood clotting. In DIC, they are depleted.

Evidence of inappropriate bleeding

Clotting times well below the normal range can indicate a hypercoagulable state.

Presence of fibrin degradation products (sometimes called fibrin split products)
Fibrin is the material that clots are made of. When antithrombin and other biochemicals remove clots, fibrin fragments become detectable. These are fibrin degradation products. A fibrin degradation product of note is called the D-Dimer. It is notable because there are in-hospital test kits that can be used to detect it. The presence of D-dimer definitely indicates that a clot has been made and broken down (though, there are many reasons for such a thing to have occurred other than DIC). A negative D-dimer test rules out DIC with 95 percent confidence.

The absence of D-Dimer rules out DIC with 95% confidence in dogs but is less reliable in cats.

Reduced fibrinogen blood levels

Fibrinogen is a fibrin precursor and the absence of it suggests that it is depleted. The use of fibrinogen reduction as a marker for DIC has been questioned because there are numerous other factors that can reduce fibrinogen.

A Special Note on Thromboelastography (TEG Testing)

In this kind of testing, a gadget called a thromboelastograph hemostasis analyzer accepts a sample of blood, forms a clot with it, and measures the strength and elasticity of the clot. The test determines if there is an excessive or reduced tendency to clot. Dogs with reduced ability to clot on the TEG test have a much higher mortality rate. This test may help determine the prognosis with DIC, at least in dogs.

Treatment

Ultimately what all this clotting and bleeding comes down to is loss of blood flow to the tissues. Treatment centers on restoring normal circulation. This means intravenous fluid administration is crucial to restore tissue perfusion. Often plasma transfusions are used to replenish consumed blood clotting proteins. Plasma is incubated with an anticoagulant substance called heparin before it is administered. Heparin activates anti-thrombin, which as mentioned has been depleted in DIC.

The most significant factor in the treatment of DIC is removal of the original disease that predisposed the patient to DIC in the first place. If this can be achieved, it would be the best chance at resolving DIC.

A house dust mite allergy is NOT a sign of a dirty house. Homes with carpeting and areas with high humidity will always have some dust mites.  

The following are some ideas that can be used to reduce the amount of house dust mites in your home.

1. House dust mites are most numerous in mattresses and beds. If possible, please keep the pet off of your bed. If this is not possible, use plastic mattress covers or some impermeable barrier for your pet’s sleeping area on the bed and wash and heat-dry bed linens weekly. Replace bedspreads, pillows and mattress covers regularly.
   
2. Feather pillows are full of house dust mites and should not be used around your allergic pet.
   
3. Pet beds should be covered in plastic, filled with cedar, or treated with insecticides inside the cover. Covers should be washed weekly and the pet beds should be aired out or put in the dryer. You should replace all pet beds every six months unless the whole bed, including the stuffing, can be laundered weekly.
   
4. When possible, choose décor and furnishings that either do not retain dust or can be easily cleaned such as: closed bookshelves instead of open shelves, washable curtains instead of blinds and heavy draperies, furniture with simple designs instead of ornately curved pieces, wooden or plastic furniture instead of upholstery, and easily cleaned decorations instead of dried flowers or straw.
   
5. Any upholstered furniture that is used by your pet should be covered with a plastic throw cloth (anti-bed-wetting mattress pads can be useful).
   
6. Stuffed pet toys should be replaced with new ones that can be laundered and dried weekly.
   
7. Vacuum and dust your pet’s environment frequently. Try to clean when the dust-sensitive pet is not at home as vacuuming and dusting stir up the allergens and increase exposure to them.
   
8. Use air conditioning or central heat to keep household humidity low. Change or clean filters on air conditioning or heating systems on a regular basis. Do not confine your pet to the laundry room, bathroom, utility room, basement or other high humidity parts of the home.
   
9. Regular use of pet flea control products is associated with lower levels of house dust mites in the home. If your pet has house dust mite allergies, we recommend that all pets in your household be kept on year-round monthly flea control.
   
10. Large amounts of house dust mites can live in carpeting. If possible, remove the carpeting in your home or keep your pet out of carpeted rooms. If your home must contain carpeting:
    • Area rugs that can be thrown into the washing machine and heat-dried once a week are preferable.
    • Sprays that breakdown the house dust mite particles that cause allergies are available but it is uncertain how effective these sprays are.

(Also called DLE, Nasal Solar Dermatitis, or Collie Nose)

Lupus – What is this Disease?

The immune system in lupus is not going around attacking every cell in the body to get to its DNA; instead, the immune system only sees DNA after cells have died and their assorted broken parts are floating around as debris. The immune system reacts to this loose DNA and generates antibodies. These antibody:DNA complexes deposit in delicate membranes, such as the kidney filtration membranes, blood vessel linings, joint capsules, and other similar structures. Once caught in these membranes, other immunologic cells are attracted and further inflammatory damage results.

Systemic lupus (SLE) involves this kind of inflammatory disruption (called a Type III hypersensitivity reaction) and the prognosis depends on which organ systems are affected and how severe the damage is. The disease is not curable but is manageable with immuno-suppressive drugs.

The name “lupus” stems from archaic times when the disease was thought to have been caused by the bite of a wolf.

Systemic Lupus Versus Discoid Lupus

DLE does not progress to SLE.

Lesions of DLE are almost always limited to the nose though they can extend up the bridge of the nose and sometimes affect the ears or inside the mouth. Early signs of the condition start with loss of nose pigment. A black nose will become bluish-grey or even pink. Scaling and cracking of the skin results and eventually, the nose will ulcerate. Exposure to sunshine makes the condition worse and there seems to be a genetic predisposition among the collie breeds (hence the term collie nose).

There are several other conditions that also cause crusts and/or erosions on the nose, so it is important to get the right diagnosis.

Some other conditions to rule out include:

• Dermatophytosis (ringworm of the nose) 
• Nasal pyoderma or Mucocutaneous pyoderma (Staph infection on the bridge of the nose)
• Pemphigus foliaceus (a different immune-mediated skin disease)
• Hyperkeratosis (a callusing disease of the nose) 
• Nasal lymphoma (a type of cancer) 
• VKH-like syndrome (another immune-mediated disease)

Diagnosis is by biopsy, which means a small piece of nose tissue must be harvested and sent to the laboratory for analysis. Most dogs will not hold still for this kind of procedure on their nose so sedation is generally needed to get proper samples.

Expect stitches afterward; some mild bleeding is possible. Diagnosis also involves some important historical information such as whether other body areas are involved, whether the condition is constant or comes and goes, and what medications have helped in the past. The pathologist will consider all of this information along with the microscopic appearance of the tissue.

Therapy Choices

For an FDA pet-approved sun protector endorsed by the Food and Drug Administration and endorsed by the American Animal Hospital Association and the SPCA, Other sun-shielding products of interest include nose shields and UV light filtering sun.

Topical Corticosteroids

The immune-suppressive effects of steroids are helpful in DLE but the systemic side effects are undesirable. Side effects are minimized by using topical steroids, typically starting twice a day and eventually dropping to an as-needed basis for maintenance after the nose is healed.

Tetracycline/Niacinamide

Tetracycline is an antibiotic with immunomodulating properties separate from its antibiotic properties. Niacinamide (also called nicotinamide) is a B vitamin supplement related to niacin (vitamin B3). The combination of these two medications has been found effective in 70% of dogs with DLE though it can take up to two months to see an effect. Treatment is given three times daily, which is relatively inconvenient for most people so alternatives have been sought. Doxycycline can be used twice a day and is frequently substituted for tetracycline.

Prednisone/Prednisolone

Oral steroids are often used to get the condition under control relatively quickly (within a month) and can be used after that as the sole therapy after the lowest effective maintenance dose is determined. Side effects include panting, excessive thirst and urination, and increased appetite. None of these effects are particularly desirable so often steroids are used in conjunction with one of the other therapies with the idea of dropping back the steroids when the second therapy can take over.

Oral Cyclosporine

Cylosporine is an immunomodulator that has found extensive use in veterinary medicine for a number of immune-mediated conditions including allergy. It can be used to control DLE but has some potential for side effects (mostly upset stomach) that might not be worthwhile for milder cases.

0.1% Tacrolimus (Protopic®)

This is a topical immunomodulator made for human use. It is very effective for use in DLE and does not cause problems if licked. Only small amounts of ointment are needed and the tube should last a long time which is good news since it is not inexpensive. The person applying the medication should wear gloves to avoid unneeded exposure.

If your dog is diagnosed with discoid lupus, discuss therapy options with your veterinarian. If your dog has a crusty or ulcerated nose, expect a biopsy to be needed to sort out the diagnosis properly before treatment can be prescribed.

Canine distemper virus can sometimes occur along with other respiratory infections, including bacterial diseases such as Bordetella bronchiseptica, and Streptococcus equi sub. zooepidemicus, fungal diseases like Mycoplasma spp., and viruses, including canine influenza virus, respiratory coronavirus, parainfluenza virus, adenovirus, and herpesvirus.

CDV is commonly spread through droplets or spray from the nose and mouth, such as through sneezing or coughing. However, infected dogs can shed the virus in nearly all bodily fluids. CDV is carried to local lymph nodes within 24 hours of contact with cells in the airways and lungs. Within a few days, the virus spreads to the spleen and abdominal lymph nodes, then spreads through the blood to cells of the gastrointestinal (GI) tract, urogenital tract, and central nervous system (CNS). The CNS tissues are typically infected by day eight or nine when neurological signs can be seen.

When the body’s immune system is triggered by exposure to disease, it reacts by producing antibodies. These antibodies are made up of proteins that attack the virus or bacteria causing the infection, hopefully protecting the body from getting sick. How strong your dog’s immune system is will play a big part in how sick they become after exposure.

If an animal’s immune system can be activated to begin making antibodies to fight CVD by the 14^th day after exposure, the signs of the illness may not be noticed.

Dogs with mild to intermediate immune responses and delayed antibody titers (this means your dog may test negative on distemper tests but still have the infection) will develop clinical signs. While the virus can eventually be cleared as antibody levels rise, it may persist for extended periods in the eye, the central nervous system (including the brain, brainstem, and spinal cord), and some skin tissues (e.g., footpads).

By days nine to 14, dogs without good immune responses tend to experience severe clinical signs and can die suddenly.

Diagnosis

Diagnostic testing starts with a physical exam and includes bloodwork, antibody tests, cytology/histopathology of affected tissues, X-rays, cerebral spinal fluid analysis, eye exams, and PCR testing. Sometimes, unfortunately, a CDV diagnosis can’t be made prior to death, and a final diagnosis can be determined only after a veterinary pathologist has examined the body.

Animals Affected By Distemper

•  cat
•  jackal
•  coyote
•  hyena
•  lion
•  tiger
•  leopard
•  ferret
•  fox
•  weasel
•  raccoon
•  seal
•  sea lion
•  dolphin
•  Giant panda
•  certain primates

Health History and Signs

Dogs with mild distemper cases may exhibit a lack of energy, decreased appetite, fever, coughing, shortness of breath, and nasal discharge.

Dogs with more severe clinical disease may show fever, nasal discharge, conjunctivitis, coughing, difficulty breathing, vomiting, diarrhea, weight loss, and dehydration. Secondary bacterial infections can occur and can make the signs worse.

Your dog may also experience signs that the central nervous system is involved, such as ataxia (incoordination), limb weakness, myoclonus (involuntary rhythmic muscle twitching), stiff neck, and hyperesthesia (skin sensitivity). These signs can occur at the same time or up to three weeks after the onset of CVD and typically get worse over time. Older dogs that have some immunity are more likely to have no signs or just mild disease.

Eye problems include keratoconjunctivitis sicca (dry eye), anterior uveitis (inflammation of the front part of the eye), and damage to the retina (which allows the brain to process sight). The optic nerves, which carry information to the brain from each eye, may develop optic neuritis (swelling and inflammation), leading to blindness.

Skin problems in puppies include pustular dermatitis (blister-like sores that can be chronic), and the skin of the nose or toe pad can develop hyperkeratosis (skin thickening). When this happens in the toe pads, it is referred to as hardpad.

Infections in puppies can cause enamel hypoplasia (damage to the developing teeth). Cardiomyopathy, or enlargement of the heart muscles, which may lead to cardiac issues, is possible. Growing puppies have developed hypertrophic osteodystrophy, (when bones in the legs grow abnormally), causing pain.

Abortion and stillbirths can occur in pregnant dogs.

Ulcers of the mouth can occur, but they tend to be rare.

Clinical signs will vary, depending on which strain of the distemper virus is involved and how well your dog’s immune system responds to the infection. Older dogs that have some immunities are more likely to have no signs or just mild disease. Puppies and animals with no immunity are more likely to have severe clinical signs.

Treatment And Management

Currently, no specific treatments are available for CDV.

Supportive care can include fluid therapy, antibiotics for secondary bacterial infections, lung treatments for bronchopneumonia, anti-nausea and vomiting medications, steroids, anti-seizure medications, etc. Supportive care will vary, depending on which parts of your dog’s body have been affected.

Prognosis

The prognosis depends on the viral strain and your dog’s immune response. Older dogs with a good immune response may not have symptoms or a mild disease. Puppies or those with a poor immune response tend to develop more severe disease.

The most important factors affecting your dog’s prognosis are neurologic. The prognosis for dogs that have neurological problems (the brain, spinal cord, and other nerves are affected) is guarded to poor, and there is a 50% chance of death. Dogs that recover may be immune to reinfection for long periods and may be immune for life.

Prevention

Hospitalized dogs with CVD must be isolated from other dogs. Dogs usually shed the virus in urine, stool, saliva, nasal mucous, etc., for one to two weeks after the initial infection. Dogs with neurologic signs can shed the virus for longer periods of time. Extended quarantine may be necessary to prevent the spread to uninfected animals.

CDV is susceptible to many disinfectants. Talk with your veterinarian about how to best disinfect areas, dishes, and toys when your dog comes home. Good hygiene practices (e.g., handwashing, wearing gloves/protective clothing) are recommended when handling infected dogs.

Vaccination

Vaccination is crucial in preventing your dog from getting CDV. Current guidelines recommend vaccinating dogs at six to eight weeks of age and repeating the vaccine every three to four weeks until the puppy is 14 to 16 weeks of age. Dogs would then receive another vaccine one year after the initial series and then every three years afterward.

Distemper antibodies that puppies could have received from their mother’s milk (colostrum) in the first few feedings, and that could prevent the vaccinations from working, are typically gone by 12-14 weeks of age. In dogs that are more than 16 weeks old, the initial vaccination series can consist of two vaccines given two to four weeks apart.

The majority of dogs develop protective antibody levels within one to two weeks following vaccination.

Zoonotic Potential

A zoonotic is a disease that can be transferred from animals to humans. There is some concern that humans might be susceptible to the canine distemper virus because of recent CDV infections in primates. Because CDV is similar to the human measles virus, additional concern has been raised because of the decrease in routine measles vaccination by many humans. However, at the time of this writing, no evidence exists that CDV can infect humans.